Research peptides · Specialized research compounds
MOTS-c
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SKUMOTS-c
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Product details
Overview
MOTS-c is a 16-amino-acid peptide associated with the mitochondrial 12S ribosomal RNA region. Research examines its role in communication between mitochondria and the nucleus and in cellular adaptation to metabolic stress.
Structure and technical data
Technical data
Format: 20 mg. Reference sequence: MRWQEMGYIFYPRKLR.
- Sequence
- MRWQEMGYIFYPRKLR
- Molecular formula
- C101H152N28O22S2
- Reported molecular mass
- 2174.6 g/mol
- CAS number
- 1627580-64-6
- PubChem CID
- 146675088
- Reported synonyms
- UNII-A5CV6JFB78
Reference molecular data.
Research context
Proposed pathways include links between the folate–methionine cycle, AICAR accumulation, and AMPK signalling. The cited studies examine muscle differentiation in vitro and the functions of pancreatic alpha and beta cells. These experimental observations are not therapeutic indications or guaranteed product outcomes.
Mitochondrial signalling and metabolic stressMuscle differentiation, YIFY, and STAT3Pancreatic cells and hormone secretionBone and remodellingNrf2, radiation, and inflammatory pain
Mitochondrial signalling and metabolic stress
MOTS-c belongs to research on mitochondria-derived peptides. The proposed folate–methionine-cycle, AICAR, and AMPK connection links nucleotide metabolism with energy sensing. Cellular location and stress conditions are essential parts of the model, not properties established from sequence alone.
Muscle differentiation, YIFY, and STAT3
The 2022 study compares MOTS-c with its Y8F variant in human LHCN-M2 and mouse C2C12 muscle cells. The reference peptide increases myotube formation, whereas the variant does not reproduce this finding. Myogenin and STAT3 transcriptional activity following IL-6 stimulation are also examined.
Pancreatic cells and hormone secretion
A 2024 study examines INS-1E beta cells and αTC-1 alpha cells. The authors report lower insulin secretion and expression in the former and greater glucagon secretion and expression in the latter. Viability, apoptosis, and responses to glucose and fatty acids are also assessed, showing a more complex picture than a generic metabolic improvement.
Bone and remodelling
Bone-metabolism literature considers the balance between formation and resorption, cell differentiation, and energy signals. The studies collected in the review distinguish osteoblasts, osteoclasts, and animal models. Links with AMPK and oxidative stress are discussed as mechanisms to evaluate within each experimental system.
Nrf2, radiation, and inflammatory pain
Separate studies examine radiation pneumonitis involving Nrf2 signalling and a mouse model of inflammatory pain hypersensitivity. Oxidative markers and lung injury matter in the former; central and peripheral pain responses in the latter.
References
- MOTS-c: A promising mitochondrial-derived peptide
- Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet dysfunction
- The Mitochondrial-Derived Peptide MOTS-c Promotes Metabolic Homeostasis and Reduces Obesity and Insulin Resistance
- MOTS-c promotes muscle differentiation in vitro
- The Mitochondrial-Derived Peptide MOTS-c Alleviates Radiation Pneumonitis via an Nrf2-Dependent Mechanism
- Central and peripheral mechanism of MOTS-c attenuates pain hypersensitivity in a mice model of inflammatory pain
- MOTS-c regulates pancreatic alpha and beta cell functions in vitro
- Role of MOTS-c in the regulation of bone metabolism
- Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging
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